This year we published simplified methods for detecting early pregnancy loss using sensitive hormone assays. Our simplified methods are already being put to use by universities and industry. Our recent studies of specific toxins have focussed on an unexplored biological pathway: prenatal exposure. We completed three studies of lasting effects in the adult linked to early exposures as a fetus. Hypotheses were suggested by animal studies of specific toxins. We found no effect of fetal exposure to mothers' smoking on the sons' later sperm characteristics (although smoking by the sons themselves seemed to decrease sperm quality). In a second study, we found no measurable effect of prenatal DES exposure on intellectual performance. In the third, there was some preliminary evidence of premature menopause among women who were exposed as fetuses to DES, suggesting that DES may be an ovarian toxin. We are incorporating molecular genetic methods into our research in order to explore the role of genetic susceptibility to environmental toxins. This year we showed that a genetic variant of the estrogen receptor (reported to be linked with miscarriage risk) had been incorrectly sequenced by previous investigators; furthermore, we found no association with miscarriage risk. The most promising area for genetic susceptibility is likely to be birth defects. In an analysis of data from the Norwegian national registry we found indirect but strong evidence that each type of birth defect has a distinct set of causes, and that these causes include environmental as well as genetic factors. These results encourage us to pursue genetic susceptibility as a major factor in environmental teratogenicity.